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The amygdalae are important, if not critical, brain regions for many affective, attentional and memorial processes, and dysfunction of the amygdalae has been a consistent finding in the study of clinical depression. Theoretical models of the functional neuroanatomy of both normal and psychopathological affective processes which posit cortical hemispheric specialization of functions have been supported by both lesion and functional neuroimaging studies in humans. Results from human neuroimaging studies in support of amygdalar hemispheric specialization are inconsistent. However, recent results from human lesion studies are consistent with hemispheric specialization. An important, yet largely ignored, feature of the amygdalae in the primate brain--derived from both neuroanatomical and electrophysiological data--is that there are virtually no direct interhemispheric connections via the anterior commissure (AC). This feature stands in stark contrast to that of the rodent brain wherein virtually all amygdalar nuclei have direct interhemispheric connections. We propose this feature of the primate brain, in particular the human brain, is a result of influences from frontocortical hemispheric specialization which have developed over the course of primate brain evolution. Results consistent with this notion were obtained by examining the nature of human amygdalar interhemispheric connectivity using both functional magnetic resonance imaging (FMRI) and positron emission tomography (PET). We found modest evidence of amygdalar interhemispheric functional connectivity in the non-depressed brain, whereas there was strong evidence of functional connectivity in the depressed brain. We interpret and discuss the nature of this connectivity in the depressed brain in the context of dysfunctional frontocortical-amygdalar interactions which accompany clinical depression.
OBJECTIVE: The anticipation of adverse outcomes, or worry, is a cardinal symptom of generalized anxiety disorder. Prior work with healthy subjects has shown that anticipating aversive events recruits a network of brain regions, including the amygdala and anterior cingulate cortex. This study tested whether patients with generalized anxiety disorder have alterations in anticipatory amygdala function and whether anticipatory activity in the anterior cingulate cortex predicts treatment response. METHOD: Functional magnetic resonance imaging (fMRI) was employed with 14 generalized anxiety disorder patients and 12 healthy comparison subjects matched for age, sex, and education. The event-related fMRI paradigm was composed of one warning cue that preceded aversive pictures and a second cue that preceded neutral pictures. Following the fMRI session, patients received 8 weeks of treatment with extended-release venlafaxine. RESULTS: Patients with generalized anxiety disorder showed greater anticipatory activity than healthy comparison subjects in the bilateral dorsal amygdala preceding both aversive and neutral pictures. Building on prior reports of pretreatment anterior cingulate cortex activity predicting treatment response, anticipatory activity in that area was associated with clinical outcome 8 weeks later following treatment with venlafaxine. Higher levels of pretreatment anterior cingulate cortex activity in anticipation of both aversive and neutral pictures were associated with greater reductions in anxiety and worry symptoms. CONCLUSIONS: These findings of heightened and indiscriminate amygdala responses to anticipatory signals in generalized anxiety disorder and of anterior cingulate cortex associations with treatment response provide neurobiological support for the role of anticipatory processes in the pathophysiology of generalized anxiety disorder.
A spiritual anthology drawn from the Greek and Russian traditions, concerned in particular with the most frequently used and best loved of all Orthodox prayers--the Jesus Prayer. Texts are taken chiefly from the letters of Bishop Theopan the Recluse, along with many other writers.
Thirty-two participants were tested for both resting electroencephalography (EEG) and neuropsychological function. Eight one-minute trials of resting EEG were recorded from 14 channels referenced to linked ears, which was rederived to an average reference. Neuropsychological tasks included Verbal Fluency, the Tower of London, and Corsi's Recurring Blocks. Asymmetries in EEG alpha activity were correlated with performance on these tasks. Similar patterns were obtained for delta and theta bands. Factor analyses of resting EEG asymmetries over particular regions suggested that asymmetries over anterior scalp regions may be partly independent from those over posterior scalp regions. These results support the notions that resting EEG asymmetries are specified by multiple mechanisms along the rostral/caudal plane, and that these asymmetries predict task performance in a manner consistent with lesion and neuroimaging studies.
The experience of aversion is shaped by multiple physiological and psychological factors including one's expectations. Recent work has shown that expectancy manipulation can alter perceptions of aversive events and concomitant brain activation. Accruing evidence indicates a primary role of altered expectancies in the placebo effect. Here, we probed the mechanism by which expectation attenuates sensory taste transmission by examining how brain areas activated by misleading information during an expectancy period modulate insula and amygdala activation to a highly aversive bitter taste. In a rapid event-related fMRI design, we showed that activations in the rostral anterior cingulate cortex (rACC), orbitofrontal cortex (OFC), and dorsolateral prefrontal cortex to a misleading cue that the taste would be mildly aversive predicted decreases in insula and amygdala activation to the highly aversive taste. OFC and rACC activation to the misleading cue were also associated with less aversive ratings of that taste. Additional analyses revealed consistent results demonstrating functional connectivity among the OFC, rACC, and insula. Altering expectancies of upcoming aversive events are shown here to depend on robust functional associations among brain regions implicated in prior work on the placebo effect.
Guided by appraisal-based models of the influence of emotion upon judgment, we propose that disgust moralizes--that is, amplifies the moral significance of--protecting the purity of the body and soul. Three studies documented that state and trait disgust, but not other negative emotions, moralize the purity moral domain but not the moral domains of justice or harm/care. In Study 1, integral feelings of disgust, but not integral anger, predicted stronger moral condemnation of behaviors violating purity. In Study 2, experimentally induced disgust, compared with induced sadness, increased condemnation of behaviors violating purity and increased approval of behaviors upholding purity. In Study 3, trait disgust, but not trait anger or trait fear, predicted stronger condemnation of purity violations and greater approval of behaviors upholding purity. We found that, confirming the domain specificity of the disgust-purity association, disgust was unrelated to moral judgments about justice (Studies 1 and 2) or harm/care (Study 3). Finally, across studies, individuals of lower socioeconomic status (SES) were more likely than individuals of higher SES to moralize purity but not justice or harm/care.
BACKGROUND: Two core characteristics of pathologic fear are its rapid onset and resistance to cognitive regulation. We hypothesized that activation of the amygdala early in the presentation of fear-relevant visual stimuli would distinguish phobics from nonphobics. METHODS: Chronometry of amygdala activation to phobia-relevant pictures was assessed in 13 spider phobics and 14 nonphobics using functional magnetic resonance imaging (fMRI). RESULTS: Blood oxygen level-dependent (BOLD) responses in the amygdala early in picture processing consistently differentiated between phobic and nonphobic subjects, as well as between phobogenic and nonphobogenic stimuli among phobics. Furthermore, amygdalar BOLD responses associated with timing but not magnitude of activation predicted affective responses to phobogenic stimuli. Computational modeling procedures were used to identify patterns of neural activation in the amygdala that could yield the observed BOLD data. These data suggest that phobic responses were characterized by strong but brief amygdala responses, whereas nonphobic responses were weaker and more sustained. CONCLUSIONS: Results are discussed in the context of the amygdala's role in rapid threat detection and the vigilance-avoidance hypothesis of anxiety. These data highlight the importance of examining the neural substrates of the immediate impact of phobogenic stimuli for understanding pathological fear.
Major depression is a heterogeneous condition, and the search for neural correlates specific to clinically defined subtypes has been inconclusive. Theoretical considerations implicate frontostriatal, particularly subgenual prefrontal cortex (PFC), dysfunction in the pathophysiology of melancholia--a subtype of depression characterized by anhedonia--but no empirical evidence has been found yet for such a link. To test the hypothesis that melancholic, but not nonmelancholic depression, is associated with the subgenual PFC impairment, concurrent measurement of brain electrical (electroencephalogram, EEG) and metabolic (positron emission tomography, PET) activity were obtained in 38 unmedicated subjects with DSM-IV major depressive disorder (20 melancholic, 18 nonmelancholic subjects), and 18 comparison subjects. EEG data were analyzed with a tomographic source localization method that computed the cortical three-dimensional distribution of current density for standard frequency bands, allowing voxelwise correlations between the EEG and PET data. Voxel-based morphometry analyses of structural magnetic resonance imaging (MRI) data were performed to assess potential structural abnormalities in melancholia. Melancholia was associated with reduced activity in the subgenual PFC (Brodmann area 25), manifested by increased inhibitory delta activity (1.5-6.0 Hz) and decreased glucose metabolism, which themselves were inversely correlated. Following antidepressant treatment, depressed subjects with the largest reductions in depression severity showed the lowest post-treatment subgenual PFC delta activity. Analyses of structural MRI revealed no group differences in the subgenual PFC, but in melancholic subjects, a negative correlation between gray matter density and age emerged. Based on preclinical evidence, we suggest that subgenual PFC dysfunction in melancholia may be associated with blunted hedonic response and exaggerated stress responsiveness.
The prefrontal cortex (PFC) has been well known for its role in higher order cognition, affect regulation and social reasoning. Although the precise underpinnings have not been sufficiently described, increasing evidence also supports a prefrontal involvement in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis. Here we investigate the PFC's role in HPA axis regulation during a psychosocial stress exposure in 14 healthy humans. Regional brain metabolism was assessed using positron emission tomography (PET) and injection of fluoro-18-deoxyglucose (FDG). Depending on the exact location within the PFC, increased glucose metabolic rate was associated with lower or higher salivary cortisol concentration in response to a psychosocial stress condition. Metabolic glucose rate in the rostral medial PFC (mPFC) (Brodman area (BA) 9 and BA 10) was negatively associated with stress-induced salivary cortisol increases. Furthermore, metabolic glucose rate in these regions was inversely coupled with changes in glucose metabolic rate in other areas, known to be involved in HPA axis regulation such as the amygdala/hippocampal region. In contrast, metabolic glucose rate in areas more lateral to the mPFC was positively associated with saliva cortisol. Subjective ratings on task stressfulness, task controllability and self-reported dispositional mood states also showed positive and negative associations with the glucose metabolic rate in prefrontal regions. These findings suggest that in humans, the PFC is activated in response to psychosocial stress and distinct prefrontal metabolic glucose patterns are linked to endocrine stress measures as well as subjective ratings on task stressfulness, controllability as well as dispositional mood states.
Developments in technologic and analytical procedures applied to the study of brain electrical activity have intensified interest in this modality as a means of examining brain function. The impact of these new developments on traditional methods of acquiring and analyzing electroencephalographic activity requires evaluation. Ultimately, the integration of the old with the new must result in an accepted standardized methodology to be used in these investigations. In this paper, basic procedures and recent developments involved in the recording and analysis of brain electrical activity are discussed and recommendations are made, with emphasis on psychophysiological applications of these procedures.
To monitor the environment for social threat humans must build affective evaluations of others. These evaluations are malleable and to a high degree shaped by responses engendered by specific social encounters. The precise neuronal mechanism by which these evaluations are constructed is poorly understood. We tested a hypothesis that conjoint activity in amygdala and fusiform gyrus would correlate with acquisition of social stimulus value. We tested this using a reinforcement learning algorithm, Q-learning, that assigned values to faces as a function of a history of pairing, or not pairing, with aversive shocks. Behaviourally, we observed a correlation between conditioning induced changes in skin conductance response (SCR) and subjective ratings for likeability of faces. Activity in both amygdala and fusiform gyrus (FG) correlated with the output of the reinforcement learning algorithm parameterized by these ratings. In amygdala, this effect was greater for averted than direct gaze faces. Furthermore, learning-related activity change in these regions correlated with SCR and subjective ratings. We conclude that amygdala and fusiform encode affective value in a manner that closely approximates a standard computational solution to learning.
Autism is a neurodevelopmental disorder affecting behavioral and social cognition, but there is little understanding about the link between the functional deficit and its underlying neuroanatomy. We applied a 2D version of voxel-based morphometry (VBM) in differentiating the white matter concentration of the corpus callosum for the group of 16 high functioning autistic and 12 normal subjects. Using the white matter density as an index for neural connectivity, autism is shown to exhibit less white matter concentration in the region of the genu, rostrum, and splenium removing the effect of age based on the general linear model (GLM) framework. Further, it is shown that the less white matter concentration in the corpus callosum in autism is due to hypoplasia rather than atrophy.
<p>This position paper advocates for early childhood teachers and parents to regularly use of mindfulness practices themselves and with very young children. An understanding of 'mindfulness' is important because it can provide ways to support children during their sensitive years and sow seeds of kindness, tolerance and peace in our fast paced, competitive, consumerist culture. In addition, in times of trauma, mindfulness techniques offer teachers and parents ways to calm themselves and the children close to them. The value of using mindfulness techniques with children and for demonstrating mindfulness as adults is well supported by research (McCown, Reibel and Micozzi, 2010; Saltzman and Goldin, 2008).</p>
Objective There is a growing scientific interest in mindfulness meditation (MM), yet its underlying neurophysiological mechanism is still uncertain. We investigated whether MM affects self-referential processing, associated with default mode network (DMN), either as short (state) – or long-term (trait) effects. Methods Three levels of MM expertise were compared with controls (n = 12 each) by electroencephalography (EEG). Results DMN deactivation was identified during the transition from resting state to a time production task, as lower gamma (25–45 Hz) power over frontal and midline regions. MM practitioners exhibited a trait lower frontal gamma activity, related to narrative self-reference and DMN activity, as well as producing longer durations, these being negatively correlated with frontal gamma activity. Additionally, we found state increases in posterior gamma power, suggesting increased attention and sensory awareness. MM proficiency did not affect the results. Conclusions Gamma power over frontal midline areas reflects DMN activity. MM practitioners exhibit lower trait frontal gamma activity, as well as a state and trait increases in posterior gamma power, irrespective of practice proficiency. Significance First, the DMN can be studied non-invasively by EEG. Second, MM induces from the early stages of practice neuroplasticity in self-referential and attentional networks.
Anxiety is a debilitating symptom of many psychiatric disorders including generalized anxiety disorder, mood disorders, schizophrenia, and autism. Anxiety involves changes in both central and peripheral biology, yet extant functional imaging studies have focused exclusively on the brain. Here we show, using functional brain and cardiac imaging in sequential brain and cardiac magnetic resonance imaging (MRI) sessions in response to cues that predict either threat (a possible shock) or safety (no possibility of shock), that MR signal change in the amygdala and the prefrontal and insula cortices predicts cardiac contractility to the threat of shock. Participants with greater MR signal change in these regions show increased cardiac contractility to the threat versus safety condition, a measure of the sympathetic nervous system contribution to the myocardium. These findings demonstrate robust neural-cardiac coupling during induced anxiety and indicate that individuals with greater activation in brain regions identified with aversive emotion show larger magnitude cardiac contractility increases to threat.
Social relations between humans critically depend on our affective experiences of others. Oxytocin enhances prosocial behavior, but its effect on humans' affective experience of others is not known. We tested whether oxytocin influences affective ratings, and underlying brain activity, of faces that have been aversively conditioned. Using a standard conditioning procedure, we induced differential negative affective ratings in faces exposed to an aversive conditioning compared with nonconditioning manipulation. This differential negative evaluative effect was abolished by treatment with oxytocin, an effect associated with an attenuation of activity in anterior medial temporal and anterior cingulate cortices. In amygdala and fusiform gyrus, this modulation was stronger for faces with direct gaze, relative to averted gaze, consistent with a relative specificity for socially relevant cues. The data suggest that oxytocin modulates the expression of evaluative conditioning for socially relevant faces via influences on amygdala and fusiform gyrus, an effect that may explain its prosocial effects.
BACKGROUND: Hypothalamic-pituitary-adrenal (HPA) system activation is adaptive in response to stress, and HPA dysregulation occurs in stress-related psychopathology. It is important to understand the mechanisms that modulate HPA output, yet few studies have addressed the neural circuitry associated with HPA regulation in primates and humans. Using high-resolution F-18-fluorodeoxyglucose positron emission tomography (FDG-PET) in rhesus monkeys, we assessed the relation between individual differences in brain activity and HPA function across multiple contexts that varied in stressfulness. METHODS: Using a logical AND conjunctions analysis, we assessed cortisol and brain metabolic activity with FDG-PET in 35 adolescent rhesus monkeys exposed to two threat and two home-cage conditions. To test the robustness of our findings, we used similar methods in an archival data set. In this data set, brain metabolic activity and cortisol were assessed in 17 adolescent male rhesus monkeys that were exposed to three stress-related contexts. RESULTS: Results from the two studies revealed that subgenual prefrontal cortex (PFC) metabolism (Brodmann's area 25/24) consistently predicted individual differences in plasma cortisol concentrations regardless of the context in which brain activity and cortisol were assessed. CONCLUSIONS: These findings suggest that activation in subgenual PFC may be related to HPA output across a variety of contexts (including familiar settings and novel or threatening situations). Individuals prone to elevated subgenual PFC activity across multiple contexts may be individuals who consistently show heightened cortisol and may be at risk for stress-related HPA dysregulation.
We investigated the top-down influence of working memory (WM) maintenance on feedforward perceptual processing within occipito-temporal face processing structures. During event-related potential (ERP) recordings, subjects performed a delayed-recognition task requiring WM maintenance of faces or houses. The face-sensitive N170 component elicited by delay-spanning task-irrelevant grayscale noise probes was examined. If early feedforward perceptual activity is biased by maintenance requirements, the N170 ERP component elicited by probes should have a greater N170 amplitude response during face relative to house WM trials. Consistent with this prediction, N170 elicited by probes presented at the beginning, middle, and end of the delay interval was greater in amplitude during face relative to house WM. Thus, these results suggest that WM maintenance demands may modulate early feedforward perceptual processing for the entirety of the delay duration. We argue based on these results that temporally early biasing of domain-specific perceptual processing may be a critical mechanism by which WM maintenance is achieved.
Reputation systems promote cooperation and deter antisocial behavior in groups. Little is known, however, about how and why people share reputational information. Here, we seek to establish the existence and dynamics of prosocial gossip, the sharing of negative evaluative information about a target in a way that protects others from antisocial or exploitative behavior. We present a model of prosocial gossip and the results of 4 studies testing the model's claims. Results of Studies 1 through 3 demonstrate that (a) individuals who observe an antisocial act experience negative affect and are compelled to share information about the antisocial actor with a potentially vulnerable person, (b) sharing such information reduces negative affect created by observing the antisocial behavior, and (c) individuals possessing more prosocial orientations are the most motivated to engage in such gossip, even at a personal cost, and exhibit the greatest reduction in negative affect as a result. Study 4 demonstrates that prosocial gossip can effectively deter selfishness and promote cooperation. Taken together these results highlight the roles of prosocial motivations and negative affective reactions to injustice in maintaining reputational information sharing in groups. We conclude by discussing implications for reputational theories of the maintenance of cooperation in human groups.